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Dr. Joanna Masel, Assistant Professor

Positions and Education
"" Assistant Professor, Ecology and Evolutionary Biology, University of Arizona, 2004-present
"" Postdoctoral Researcher, Biological Sciences, Stanford University 2000-2003
"" D. Phil. Zoology, Oxford University 2001
"" B.Sc. (Hons) University of Melbourne 1996
Honors and Awards

"" Pew Scholar in the Biomedical Sciences, 2007
"" Alfred P. Sloan Research Fellow, 2007
Merton College Prize Scholarship, 1999
Rhodes Scholarship, 1997
International Mathematical Olympiad: Bronze Medal, 1991


Visit the Masel Group website here for more detailed information.
Research Interests

I am a theoretical or mathematical biologist. The fields I work in are very diverse. They tend to involve complex systems far from equilibrium, whose emergent properties are not immediately obvious from their component parts.

One question I find interesting is how the rate of evolution can itself evolve. Systems known as evolutionary capacitors are able to store variation in a latent form, releasing it only when necessary. The yeast prion [PSI+] and the heat shock protein Hsp90 are good examples of such systems. I use both theoretical population genetics and bioinformatics / comparative genomics to study evolutionary capacitance. For example, why is latent variation not packed full of lethal alleles? The theoretical answer is that latent variation is only 95% latent not 100% latent, and this is enough to screen out most lethal alleles. The comparative genomic approach is then to look for evidence for that 5% expression, for example in the 3'UTR sequences revealed by [PSI+]. I analyze how specific capacitor systems have evolved in the past, predict how capacitance properties should evolve in general, and study how capacitance affects the overall rate of evolution.

In collaboration with Mark Siegal at NYU, I also model networks of transcriptional regulators in order to study the evolutionary properties of canalization (also known as robustness) and genetic assimilation. Robustness that is the product of evolution can have very different properties to robustness that is the product of an engineering process. Complex interacting networks can also act as evolutionary capacitors by concealing and revealing variation. We are constructing a model of gene networks that is both realistic enough to be related to data and simple enough for experimental evolution to be rapidly simulated. This tool will open up a range of questions relating the evolution of robustness to the stochasticity associated with small numbers of molecules in cells.

Another interest is how prions, which lack any DNA or RNA, are able to replicate. The incubation period of prion diseases is incredibly precise, leading to high quality in vivo data. I develop mathematical models of prion replication and compare them to data on prion incubation times. This allows us to study how prions replicate and how best to interfere with this replication.

Past interests currently on the backburner include intrahost dynamics of HIV and psychological approaches to explain the level of cooperation observed when humans act out the dilemmas of game theory.

Read a profile of Joanna Masel in the Fall 2004 (Winter 2005) issue of Desert News & Views (pdf file)

PubMed list of publications for Joanna Masel
Selected Publications
  1. King, O.D., Masel, J. (2007) The evolution of bet-hedging in finite populations, Theor Pop Biol in press.

  2. Giacomelli, M., Hancock, A., Masel, J. (2007) The conversion of 3' UTRs into coding regions. Molecular Biology & Evolution, 24:457-464.

  3. Masel, J., King, O.D., Maughan, H. (2007) The loss of adaptive plasticity during long periods of environmental stasis. The American Naturalist 169:38-46.

  4. Maughan, H., Masel, J., Birky, C. W., & Nicholson, W. L. (2007). The role of mutation accumulation and selection in loss of sporulation in experimental populations of Bacillus subtilis. Genetics, in press.

  5. Masel, J., Maughan H. (2007) Mutations leading to loss of sporulation ability in Bacillus subtilis are sufficiently frequent to favor genetic canalization. Genetics 175:453-457.

  6. Maughan, H., Callicotte, V., Hancock, A., Birky, C.W., Nicholson, W.L., Masel, J. (2006) The population genetics of phenotypic deterioration in experimental populations of Bacillus subtilis, Evolution, 60, 686-695.

  7. Masel, J., (2006) Cryptic genetic variation is enriched for potential adaptations, Genetics 172, 1985-1991.

  8. Masel, J., (2005) Evolutionary capacitance may be favored by natural selection. Genetics 170: 1359-1371.

  9. Masel, J. (2004) Genetic assimilation can occur in the absence of selection for the assimilating phenotype, suggesting a role for the canalization heuristic. J. Evol. Biol., 17, 1106-1110.

  10. Masel, J., Bergman, A. (2003) The evolution of the evolvability properties of the yeast prion [PSI+]. Evolution, 57, 1498-1512.

  11. Masel, J. (2007) A Bayesian model of quasi-magical thinking can explain observed co-operation in the public good game. In Press, J. Econ. Behav. Organ.

  12. Masel, J., Genoud, N., Aguzzi, A., (2005) Efficient inhibition of prion replication by PrP-Fc2 suggests that the prion is a PrPSc oligomer. J. Mol. Biol., 345, 1243-1251.

  13. Masel, J., Jansen, V.A.A., (2001). The measured level of prion infectivity varies in a predictable way according to the aggregation state of the infectious agent. Biochim. Biophys. Acta, 1535 pp.164-173.

  14. Masel, J., Jansen, V.A.A., (2000). Designing drugs to stop the formation of prion aggregates and other amyloids. Biophys. Chem., 88, 47-59.

  15. Masel, J., Jansen, V.A.A., Nowak, M.A. (1999). Quantifying the kinetic parameters of prion replication. Biophys. Chem., 77, 139-152.
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